Polysomnography in patients with post‐traumatic stress disorder

Aims: The purpose of the present study was to investigate sleep structure in post‐traumatic stress disorder (PTSD) patients with and without any psychiatric comorbidities. The relationship between sleep variables and measurements of clinical symptom severity were also investigated. Methods: Sleep patterns of 24 non‐medicated male PTSD patients and 16 age‐ and sex‐matched normal controls were investigated on polysomnography on two consecutive nights. Six PTSD‐only patients and 15 PTSD patients with major depressive disorder (MDD) were also compared to normal controls. Sleep variables were correlated with PTSD symptoms. Results: Compared to the normal controls, the PTSD patients with MDD had difficulty initiating sleep, poor sleep efficiency, decreased total sleep time, decreased slow wave sleep (SWS), and a reduced rapid eye movement (REM) sleep latency. The PTSD patients without any comorbid psychiatric disorders had moderately significant disturbances of sleep continuity, and decreased SWS, but no abnormalities of REM sleep. REM sleep latency was inversely proportional to the severity of startle response. SWS was found to be inversely correlated with the severity of psychogenic amnesia. Conclusions: PTSD patients have disturbance of sleep continuity, and SWS deficit, without the impact of comorbid depression on sleep. The relationship between SWS and the inability to recall an important aspect of trauma may indicate the role of sleep in the consolidation of traumatic memories. The relationship between the severity of the startle response and REM latency may suggest that REM sleep physiology shares common substrates with the symptoms of PTSD.     

Post-traumatic stress disorder and sleep-what a nightmare!

According to DSM IV criteria, sleep disturbances are incorporated in the definition of post-traumatic stress disorder (PTSD). These include the re-experiencing symptoms (nightmares, criteria B) and a hyperarousal state (difficulty initiating and maintaining sleep, criteria D). PTSD patients commonly complain of sleep disturbances. Moreover, insomnia, restless sleep and trauma-related dreams might be the primary complaint of some patients. However, although subjective sleep disturbances are considered characteristic of PTSD, sleep laboratory studies have provided inconsistent evidence of objective sleep disorders. A variety of sleep architectures and sleep patterns has been reported in PTSD. However, only a few studies have controlled for comorbidities. Thus, uncertainty exists to what extent the sustained complaints of sleep disturbances in chronic PTSD are specifically related to the impact of exposure to traumatic stress, or rather are a consequence of comorbid disorders. Specific changes in REM sleep suggest a pathophysiologic role of REM sleep abnormality in PTSD (e.g. anxiety dreams, increased REM density, exaggerated startle response, decreased dream recall and elevated awakening thresholds from REM sleep). However, again, studies have failed to show consistent changes in percentage of REM sleep or in REM latency. There might be a coexistence of pressure to REM along with inhibitory forces of REM that result in high variability of REM parameters across patients. Alternatively, changes in REM sleep might reflect the effect of comorbid psychiatric disorders that results in inconsistent findings between patients. The current review tries to address these issues based on recent studies carried out in this field.     

Sleep findings in young adult patients with posttraumatic stress disorder.

BACKGROUND: Laboratory sleep studies in posttraumatic stress disorder (PTSD) have not provided consistent evidence of sleep disturbance, despite apparent sleep complaints. Most of these studies have investigated middle-aged chronic PTSD subjects with a high prevalence of comorbidities such as substance dependence and/or personality disorder. METHODS: Ten young adult PTSD patients (aged 23.4 +/- 6.1 years) without comorbidities of substance dependence and/or personality disorder underwent 2-night polysomnographic recordings. These sleep measures were compared with those of normal control subjects and were correlated with PTSD symptoms. RESULTS: Posttraumatic stress disorder patients demonstrated significantly poorer sleep, reduced sleep efficiency caused by increased wake time after sleep onset, and increased awakening from rapid eye movement (REM) sleep (REM interruption). We found significant positive correlations between the severity of trauma-related nightmare complaints and the percentage of REM interruption, as well as wake time after sleep onset. CONCLUSIONS: The results indicate that trauma-related nightmares are an important factor resulting in increased REM interruptions and wake time after sleep onset in PTSD.     

Stress-induced changes in sleep in rodents: models and mechanisms

Psychological stressors have a prominent effect on sleep in general, and rapid eye movement (REM) sleep in particular. Disruptions in sleep are a prominent feature, and potentially even the hallmark, of posttraumatic stress disorder (PTSD) (Ross, R.J., Ball, W.A., Sullivan, K., Caroff, S., 1989. Sleep disturbance as the hallmark of posttraumatic stress disorder. American Journal of Psychiatry 146, 697-707). Animal models are critical in understanding both the causes and potential treatments of psychiatric disorders. The current review describes a number of studies that have focused on the impact of stress on sleep in rodent models. The studies are also in Table 1, summarizing the effects of stress in 4-h blocks in both the light and dark phases. Although mild stress procedures have sometimes produced increases in REM sleep, more intense stressors appear to model the human condition by leading to disruptions in sleep, particularly REM sleep. We also discuss work conducted by our group and others looking at conditioning as a factor in the temporal extension of stress-related sleep disruptions. Finally, we attempt to describe the probable neural mechanisms of the sleep disruptions. A complete understanding of the neural correlates of stress-induced sleep alterations may lead to novel treatments for a variety of debilitating sleep disorders.     

A window into the invisible wound of war: Functional neuroimaging of REM sleep in returning combat veterans with PTSD

Relative regional cerebral metabolic rate of glucose in rapid eye movement (REM) sleep and wakefulness was explored in combat veterans with and without posttraumatic stress disorder PTSD, using positron emission tomography. Hypermetabolism in brain regions involved in arousal regulation, fear responses, and reward processing persist during REM sleep in combat veterans with PTSD.     

REM sleep and the early development of posttraumatic stress disorder

OBJECTIVE: The potential for chronicity and treatment resistance once posttraumatic stress disorder (PTSD) has become established has stimulated interest in understanding the early pathogenesis of the disorder. Arousal regulation and memory consolidation appear to be important in determining the development of PTSD; both are functions of sleep. Sleep findings from patients with chronic PTSD are complex and somewhat contradictory, and data from the acute phase are quite limited. The aim of the present study was to obtain polysomnographic recordings during an acute period after life-threatening experiences and injury and to relate measures of sleep duration and maintenance and the timing, intensity, and continuity of REM sleep to the early development of PTSD. METHOD: Twenty-one injured subjects meeting study criteria received at least one polysomnographic recording close to the time of medical/surgical stabilization and within a month of injury. PTSD symptoms were assessed concurrently and 6 weeks later. Sleep measures were compared among injured subjects with and without significant PTSD symptoms at follow-up and 10 noninjured comparison subjects and were also correlated with PTSD severity. RESULTS: There was more wake time after the onset of sleep in injured, trauma-exposed patients than in noninjured comparison subjects. Development of PTSD symptoms was associated with shorter average duration of REM sleep before a stage change and more periods of REM sleep. CONCLUSIONS: The development of PTSD symptoms after traumatic injury is associated with a more fragmented pattern of REM sleep.     

Sleep pathophysiology in posttraumatic stress disorder and idiopathic nightmare sufferers.

BACKGROUND: Nightmares are common in posttraumatic stress disorder (PTSD), but they also frequently occur in idiopathic form. Findings associated with sleep disturbances in these two groups have been inconsistent, and sparse for idiopathic nightmares. The aim of the present study was to investigate whether sleep anomalies in PTSD sufferers with frequent nightmares (P-NM) differ from those observed in non-PTSD, idiopathic nightmare (I-NM) sufferers and healthy individuals. METHODS: Sleep measures were obtained from nine P-NM sufferers, 11 I-NM sufferers, and 13 healthy control subjects. All participants slept in the laboratory for two consecutive nights where electroencephalogram, electro-oculogram, chin and leg electromyogram, electrocardiogram, and respiration were recorded continuously. RESULTS: Posttraumatic nightmare sufferers had significantly more nocturnal awakenings than did I-NM sufferers and control subjects. Elevated indices of periodic leg movements (PLMs) during rapid eye movement (REM) and non-REM sleep characterized both P-NM and I-NM sufferers. CONCLUSIONS: Posttraumatic nightmare sufferers exhibit more nocturnal awakenings than do I-NM sufferers and control subjects, which supports the hypothesis of hyperarousal in sleep in PTSD sufferers; however, elevated PLM indices in both P-NM and I-NM sufferers suggest that PLMs may not be a marker of hyperarousal in sleep of PTSD sufferers. Rather, PLMs may be a correlate of processes contributing to intense negative dreaming.     

Clinical presentation of PTSD in World War II combat veterans.

Clinicians have increasingly recognized posttraumatic stress disorder (PTSD) among Vietnam veterans, but the disorder may be easily overlooked among World War II combat veterans. The authors review recent studies of PTSD in older veterans and describe five cases that illustrate the diverse clinical presentations of PTSD in this population. Symptoms included anxiety, cognitive and somatic complaints, depression, alcohol dependence, and amnestic periods. Despite the varied presentations, a fairly consistent patient profile emerged. Patients avoided reminders of war, showed an exaggerated startle response, and experienced restless sleep and chronic anxiety. Factors associated with exacerbations of symptoms were retirement and reminders of war experiences. Although past studies have emphasized resuppression of the trauma, the authors encourage a flexible approach to treatment, including exploratory techniques.     

Toward rational pharmacotherapy for posttraumatic stress disorder: an interim report

There is growing evidence that medication can alleviate symptoms associated with posttraumatic stress disorder (PTSD). Recent research also suggests that PTSD has a unique biological profile consisting of alterations in sympathetic arousal, the neuroendocrine system, and the sleep/dream cycle. This profile distinguishes PTSD from both major depression and panic disorder. Medication appears to alleviate PTSD symptoms associated with sympathetic hyperarousal and intrusive recollections of the trauma but seems ineffective against avoidant symptoms. Pharmacotherapy alone is rarely sufficient to provide complete remission of PTSD. Symptom relief provided by medication facilitates the patient's participation in individual, behavioral, or group psychotherapy.     

Sleep in a community sample of elderly war veterans with and without posttraumatic stress disorder.

BACKGROUND: Although sleep disturbances are commonly reported by individuals with posttraumatic stress disorder (PTSD), objective findings have been inconsistent, due in part to small sample sizes, comorbid psychiatric disorders, variations in the recentness of trauma exposure, and the use of PTSD subjects involved in psychiatric treatment. METHODS: A community sample of elderly males (n = 59) exposed to war trauma 28-50 years ago and free from sleep-affecting medications and disorders other than PTSD completed 3 nights of polysomnography. Of these participants, 30 met criteria for current PTSD; three were receiving supportive outpatient psychotherapy. RESULTS: Two statistically significant differences were observed: Those with PTSD had a higher percentage of rapid eye movement (REM) sleep and fewer arousals from non-REM sleep. The perceptions of sleep quality among the participants with PTSD were lower than the perceptions of non-PTSD participants. Although participants with untreated obstructive sleep apnea and sleep movement disorders were not included in the sample, many cases were detected on initial screening. Treatment resulted in improved sleep and increased feelings of well being. CONCLUSIONS: Alterations in REM and arousals characterized PTSD in this sample. When comorbid sleep disorders were ruled out, sleep was clinically similar across the groups. Trauma-related sleep disturbances that subjects reported as arising early in the course of the disorder appear to have declined over time.     

Temporal relations between sleep problems and both traumatic event exposure and PTSD: A critical review of the empirical literature

There has been growing interest in the interrelations among traumatic event exposure, posttraumatic stress disorder (PTSD), and sleep problems. A wealth of research has examined the associations among these factors and there is an emerging literature focused on how sleep problems relate to both traumatic event exposure and PTSD across time. The current review provides a detailed analysis of studies pertaining to the temporal patterning of sleep problems and traumatic event-related factors (e.g., traumatic event exposure, PTSD) and draws conclusions regarding the current state of this literature. Research coalesces to suggest (1) exposure to a traumatic event can interfere with sleep, (2) PTSD is related to the development of self-reported sleep problems, but evidence is less clear regarding objective indices of sleep, and (3) limited evidence suggests sleep problems may interfere with recovery from elevated posttraumatic stress levels. Future research now needs to focus on understanding mechanisms involved in these patterns to inform the prevention and treatment of comorbid sleep problems and PTSD.     

Magnetic resonance findings in REM sleep behavior disorder

Rapid eye movement (REM) sleep behavior disorder is characterized by bizarre acts during nocturnal sleep that may lead to physical injuries. Dream content suggests that motor overactivity is an attempted dream enactment and polygraphic studies reveal REM stage without atonia, an alteration of REM sleep generation that facilitates excessive motor activity. In 6 patients with REM sleep behavior disorder. MRI of the brain showed multifocal signal intensity lesions suggestive of lacunar infarcts in periventricular regions (5 patients) and in dorsal pontomesencephalic areas (3 patients). REM sleep behavior disorder may be the result of injury to the midrostral tegmentum nuclei, the tegmentoreticular tracts, or both. This condition is easily controlled with clonazepam.     

Sleep in lifetime posttraumatic stress disorder: a community-based polysomnographic study

BACKGROUND: Sleep complaints are common in posttraumatic stress disorder (PTSD) and are included in the DSM criteria. Polysomnographic studies conducted on small samples of subjects with specific traumas have yielded conflicting results. We therefore evaluated polysomnographic sleep disturbances in PTSD. METHODS: A representative cohort of young-adult community residents followed-up for 10 years for exposure to trauma and PTSD was used to select a subset for sleep studies for 2 consecutive nights and the intermediate day. Subjects were selected from a large health maintenance organization and are representative of the geographic area except for the extremes of the socioeconomic status range. The subset for the sleep study was selected from the 10-year follow-up of the cohort (n = 913 [91% of the initial sample]). Eligibility criteria included (1) subjects exposed to trauma during the preceding 5 years; (2) others who met PTSD criteria; and (3) a randomly preselected subsample. Of 439 eligible subjects, 292 (66.5%) participated, including 71 with lifetime PTSD. Main outcomes included standard polysomnographic measures of sleep induction, maintenance, staging, and fragmentation; standard measures of apnea/hypopnea and periodic leg movement; and results of the multiple sleep latency test. RESULTS: On standard measures of sleep disturbance, no differences were detected between subjects with PTSD and control subjects, regardless of history of trauma or major depression in the controls. Persons with PTSD had higher rates of brief arousals from rapid eye movement (REM) sleep. Shifts to lighter sleep and wake were specific to REM and were significantly different between REM and non-REM sleep (F(1,278) = 5.92; P =.02). CONCLUSIONS: We found no objective evidence for clinically relevant sleep disturbances in PTSD. An increased number of brief arousals from REM sleep was detected in subjects with PTSD. Sleep complaints in PTSD might represent amplified perceptions of brief arousals from REM sleep.     

Heart rate variability during sleep and the early development of posttraumatic stress disorder

Background

Noradrenergic function has been linked to posttraumatic stress disorder (PTSD) and might have a role in mediating sleep disturbances of the disorder. Our objective was to relate a peripheral manifestation of noradrenergic function, sympathetic nervous system activity as indexed by heart rate variability during sleep, to the development of PTSD in subjects with recent traumatic injuries.

Methods

Subjects who had recall of life-threatening experiences were recruited from one of two regional trauma centers. Select subjects received a polysomnographic recording within 1 month of the trauma. Digitized electrocardiogram recordings were extracted from early and late rapid-eye-movement (REM) and preceding non-REM sleep periods. Autoregression was applied to R-R interval time series to calculate the ratios of low-frequency to high-frequency spectral densities (LF/HF ratios), which index sympathetic activation. Posttraumatic stress disorder status was determined at 2 months.

Results

There was a significant state × group interaction: LF/HF ratios were higher during the REM sleep of the nine subjects who were positive for PTSD symptoms, compared with the 10 subjects who were PTSD negative.

Conclusions

Our findings are consistent with the possibility that increased noradrenergic activity during REM sleep contributes to the development of PTSD.     

Sleep in Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) is often associated with sleep disturbances. In this review, we focus on the published literature on subjective and objective findings of sleep in patients with PTSD. Insomnia and nightmares are most commonly reported subjective sleep disturbances. Polysomnographic investigations have frequently reported rapid eye movement (REM) sleep abnormalities in PTSD. However, studies have not been consistent about the type of REM sleep dysfunction in PTSD patients. Antidepressants such as nefazodone, trazodone, fluvoxamine, and imagery rehearsal therapy are found to be beneficial in the treatment of PTSD associated sleep disturbances as well as core symptoms of this anxiety disorder. We propose use of such modalities of treatment in PTSD patients with predominant sleep disturbances. Further studies are required to clarify polysomnographic sleep changes especially role of REM sleep dysregulation and treatment of sleep disturbances in PTSD.     

Do all mammals dream?

The presence of dreams in human sleep, especially in REM sleep, and the detection of physiologically similar states in mammals has led many to ponder whether animals experience similar sleep mentation. Recent advances in our understanding of the anatomical and physiological correlates of sleep stages, and thus dreaming, allow a better understanding of the possibility of dream mentation in nonhuman mammals. Here, we explore the potential for dream mentation, in both non-REM and REM sleep across mammals. If we take a hard-stance, that dream mentation only occurs during REM sleep, we conclude that it is unlikely that monotremes, cetaceans, and otariid seals while at sea, have the potential to experience dream mentation. Atypical REM sleep in other species, such as African elephants and Arabian oryx, may alter their potential to experience REM dream mentation. Alternatively, evidence that dream mentation occurs during both non-REM and REM sleep, indicates that all mammals have the potential to experience dream mentation. This non-REM dream mentation may be different in the species where non-REM is atypical, such as during unihemispheric sleep in aquatic mammals (cetaceans, sirens, and Otariid seals). In both scenarios, the cetaceans are the least likely mammalian group to experience vivid dream mentation due to the morphophysiological independence of their cerebral hemispheres. The application of techniques revealing dream mentation in humans to other mammals, specifically those that exhibit unusual sleep states, may lead to advances in our understanding of the neural underpinnings of dreams and conscious experiences.     

Stress-induced enhancement of auditory startle: an animal model of posttraumatic stress disorder

An innovative animal model of posttraumatic stress disorder (PTSD) is proposed in which nonhabituation of the acoustic startle response is developed in rats subsequent to tailshock exposure. Subjects (n = 31) received 30 minutes of intermittent tail shock on 2 days followed by exposure to the tailshock apparatus on the third day. Compared to baseline startle reactions, 9 of 31 tailshock-exposed rats developed nonhabituation of startle response reactions during the subsequent 3 weeks of testing. No control rats developed nonhabituation of startle reactions over a similar time period. These data suggest that this system models useful aspects of clinical PTSD emphasizing nonhabituation of startle reactions as a dependent variable. The method consistently identifies a subgroup of rats that develop persistent nonhabituation of startle in response to a tailshock-stress paradigm.     

Startle reactivity in the long-term after severe accidental injury: Preliminary data

An exaggerated startle response is one of the core hyperarousal symptoms of posttraumatic stress disorder (PTSD). Heightened startle eye-blink magnitude and reduced habituation of this response in PTSD patients have been reported in several studies. However, it is unclear whether this is an enduring characteristic of individuals vulnerable for PTSD or to which degree trauma-exposed individuals who do not develop PTSD also show exaggerated startle. Thirteen accident survivors with remitted PTSD, 12 trauma controls, and 16 non-trauma controls were examined. Four measures of startle reactivity were analyzed in response to 15 bursts of white noise (95 dB, 50 ms): eye-blink magnitude, eye-blink onset latency, skin conductance response, and heart rate response. The eye-blink reflex was measured over the left musculus orbicularis oculi. Reactivity and habituation were analyzed using linear mixed models. Remitted PTSD subjects did not differ from non-trauma controls regarding any of the startle reactivity or habituation measures. Unexpectedly, trauma controls showed larger eye-blink magnitude than non-trauma controls. These results suggest that the exaggerated startle response disappears after remission from PTSD. Further, they suggest that psychologically resilient trauma survivors might show a PTSD-like pattern of exaggerated physiological startle even many years after a traumatic event.     

The neural correlates and temporal sequence of the relationship between shock exposure, disturbed sleep and impaired consolidation of fear extinction

Consolidation of extinction learning is a primary mechanism disrupted in posttraumatic stress disorder (PTSD), associated with hypoactivity of the ventromedial prefrontal cortex and hippocampus. A role for rapid eye movement (REM) sleep disturbances in this failure to consolidate extinction learning has been proposed. We performed functional magnetic resonance imaging (fMRI) with simultaneous skin conductance response (SCR) measurements in 16 healthy participants during conditioning/extinction and later recall of extinction. The visual stimuli were basic geometric forms and electrical shocks functioned as the unconditioned stimulus. Between the conditioning/extinction and recall sessions, participants received a 90-min sleep window in the sleep laboratory. This daytime sleep was polysomnographically recorded and scored by professionals blind to the study design. Only seven out of 16 participants had REM sleep; participants without REM sleep had a significantly slower decline of both SCR and neural activity of the laterodorsal tegmentum in response to electrical shocks during conditioning. At recall of fear extinction, participants with preceding REM sleep had a reduced SCR and stronger activation of the left ventromedial prefrontal cortex and bilateral lingual gyrus in response to the extinguished stimulus than participants lacking REM sleep. This study indicates that trait-like differences in shock reactivity/habituation (mediated by the brainstem) are predictive of REM sleep disruption, which in turn is associated with impaired consolidation of extinction (mediated by the ventromedial prefrontal cortex). These findings help understand the neurobiological basis and the temporal sequence of the relationship between shock exposure, disturbed sleep and impaired consolidation of extinction, as observed in PTSD.     

La motricité redevient-elle normale en sommeil paradoxal ? Le trouble comportemental en sommeil paradoxal

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by violent, or potentially violent, movements during REM sleep, corresponding to enacted dreams. During sleep monitoring, there is a partial or total loss of the normal muscle atonia during REM sleep. REM sleep behavior disorder predominantly affects elderly subjects without any other disease (idiopathic RBD, a precursor of Parkinson disease and Lewy body dementia) or suffering from various neurological and neurodegenerative diseases, mainly synucleinopathies. In addition to being a treatable cause of nocturnal injury of the patients or their bed-partners, RBD is a fantastic window into motor and cognitive control during REM sleep. Notably, parkinsonism transiently disappears during RBD. The patient's voice is louder and better articulated than when awake, and movements are rapid (but jerky) suggesting that the deleterious message from the basal ganglia to the primary motor cortex is reduced or bypassed. As we observed culturally-acquired behaviors, retired patients practicing their former work with mastered gestures, as well as sentences pronounced with appropriate prosody, gesturing, fluency, and syntax during the RBD, we suggest that these behaviors are generated by the same cortical areas as during wakefulness. This model also enables the demonstration that REM during REM sleep are coded in the same direction as the arm and hand movements, as if the dreamer were scanning the dream images. This online access to the motor and verbal dream scenario (through the video and audio monitoring), and the physiological measures (via the EEG, eye movements, muscle tone, respiration, heart rate), together with the offline access to the mental content (dream report after the awakening) constitute a triangulation for validating new hypotheses about REM sleep and dreams.